Some patients with lung disease retain CO2, while others with similar lung function do not. This could be explained if CO2 retainers had a pre-existing low hypercapnic ventilatory response (HCVR) and, from this, a tendency to retain CO2. To test if such a phenomenon exists in healthy people, we determined the change in end-tidal PCO2 (ΔPETCO2) produced by the addition of a dead-space (DS), during wakefulness and sleep, and related this to the HCVR measured awake. The group mean (n=14) HCVR slope was 2.2±1.1 (S.D.) L min-1 mmHg-1. The ΔPETCO2 with the application of DS was 1.6±1.6 mmHg awake and 2.6±2.2 mmHg asleep. During wakefulness the ?PETCO2 with DS did not correlate with the HCVR slope. However, during sleep, four subjects had a marked increase in the ΔPETCO2 (3.7, 4.3, 6.2, 8.0 mmHg) and a relatively low HCVR (slope 1.5, 1.7, 1.5, 1.7 L min-1 mmHg-1, respectively). We speculate that such individuals, should they develop lung disease, may be predisposed to retain CO2. © 2003 Elsevier Science B.V. All rights reserved.
- Carbon dioxide, retention, lung disease
- Control of breathing, hypercapnic ventilatory response
- Dead space, added external, CO2 retention
- Mammals, humans